Morbid obesity, sleep apnea, obesity hypoventilation syndrome: Are we sleepwalking into disaster?

Morbid obesity, sleep apnea, obesity hypoventilation syndrome: Are we sleepwalking into disaster?

Author’s Accepted Manuscript Morbid Obesity, Sleep Apnea, Obesity Hypoventilation Syndrome: Are We Sleepwalking Into Disaster? Raviraj Raveendran, Jea...

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Author’s Accepted Manuscript Morbid Obesity, Sleep Apnea, Obesity Hypoventilation Syndrome: Are We Sleepwalking Into Disaster? Raviraj Raveendran, Jean Wong, Frances Chung www.elsevier.com/locate/jcomm

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S2405-6030(17)30045-6 https://doi.org/10.1016/j.pcorm.2017.11.010 PCORM52

To appear in: Perioperative Care and Operating Room Management Received date: 6 October 2017 Accepted date: 2 November 2017 Cite this article as: Raviraj Raveendran, Jean Wong and Frances Chung, Morbid Obesity, Sleep Apnea, Obesity Hypoventilation Syndrome: Are We Sleepwalking Into Disaster?, Perioperative Care and Operating Room Management, https://doi.org/10.1016/j.pcorm.2017.11.010 This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting galley proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.

Morbid Obesity, Sleep Apnea, Obesity Hypoventilation Syndrome: Are We Sleepwalking Into Disaster? Raviraj Raveendran. MBBS, FANZCA Consultant Anesthesiologist, Department of Anesthesiology, Palmerston North Hospital, Mid Central District Health Board, Palmerston North, New Zealand [email protected] Jean Wong MD FRCPC Associate Professor, Department of Anesthesiology, Toronto Western Hospital, University Health Network, University of Toronto [email protected] Frances Chung. MBBS FRCPC Professor, Department of Anesthesiology, Toronto Western Hospital, University Health Network, University of Toronto [email protected] (Corresponding Author) Based on a presentation given at the 12th Annual Perioperative Medicine Summit (March 9th, 2017), Fort Lauderdale, FL.

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Abstract An increase in the prevalence of obesity globally has been associated with the increase in sleep disordered breathing conditions (SBD) like obstructive sleep apnea and obesity hypoventilation syndrome. These high-risk patients are prone for increased perioperative morbidity and mortality because

of

associated

comorbid

conditions,

difficult

intubation

and

postoperative

cardiorespiratory complications. However, a significant number of patients with SDB are not diagnosed at the time of surgery due to lack of awareness among perioperative team members. Identification of these high-risk patients and optimizing them preoperatively may improve the perioperative outcome. Various perioperative organizations have made guidelines on managing patients with morbid obesity and sleep disordered breathing. Every hospital should have a written policy on preoperative assessment, intraoperative and postoperative management of obese patients with sleep disordered breathing.

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Introduction Obesity is a chronic, multisystem, proinflammatory disorder. Obesity is defined as a body mass index (BMI) >30 kg/m2; morbid obesity is defined as a BMI >35 kg/m2; super morbid obesity BMI >50 kg/m2 and ultra-obesity BMI >70 kg/m2. The recent increase in obesity in various parts of the world has been termed ‘globesity’. The prevalence of obesity among adults in the United States is 34.9 % and the prevalence of morbid obesity is 6.3 %.1 Obesity is an important risk factor for sleep disordered breathing (SBD) conditions like obstructive sleep apnea (OSA) and obesity hypoventilation syndrome (OHS). SBD is associated with various comorbidities such as myocardial ischemia, heart failure, hypertension, arrhythmias, metabolic syndrome, insulin resistance, cerebrovascular disease, and gastroesophageal reflux. Patients with OSA and OHS are prone to perioperative complications posing challenges for the perioperative management. A significant number of patients with OSA and OHS are undiagnosed when they present for elective surgery.2 To improve the perioperative outcomes, various guidelines have been published for these high-risk patients.3,4,5,6,7 However, a recent nationwide survey in the United States on attitudes regarding perioperative care showed that only 27% of the hospitals have written policies for the perioperative care of patients with OSA.8 The purpose of this review is to provide an update of evidence on the perioperative management of morbid obesity, OSA and OHS.

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Obstructive sleep apnea Obstructive sleep apnea is the most common type of sleep disordered breathing. OSA is a disease characterized by recurrent episodic cessation of breathing lasting ≥ 10 sec during sleep. The severity of OSA is identified by the apnea hypopnea index (AHI), defined as the number of abnormal breathing events per hour of sleep. Apnea is a reduction of airflow of ≥ 90% of baseline for ≥ 10 sec, while hypopnea is considered a decrease in airflow by ≥ 30% baseline for ≥ 10 sec in association with either ≥ 3% oxygen desaturation from pre-event baseline and/or the event is associated with an arousal.9 The American Academy of Sleep Medicine (AASM) criteria for diagnosing OSA requires either an AHI ≥15, or AHI ≥5 events/hr with symptoms such as daytime sleepiness, loud snoring, or observed obstruction during sleep.10 The severity of OSA is graded as mild, moderate and severe with AHI ≥ 5 to < 15, AHI ≥ 15 to ≤ 30, and AHI > 30 events/hr respectively. 10

In general, sleep reduces the upper airway muscle tone leading to an enhanced collapsibility, which is more pronounced during REM sleep. This normal physiological alteration is exaggerated in OSA patients. OSA may be due to excess soft tissue of the upper airway with a normal skeletal frame (obesity) or normal soft tissue of the upper airway with a restricted skeletal frame (craniofacial abnormality). The prevalence of OSA in the general population aged 30 to 70 years is 5% in women and 14% in men,11 and is 78% in morbidly obese patients undergoing bariatric surgery.12 The incidence of OSA increases with age and males have a threefold increased risk for OSA. Craniofacial abnormalities including short mandibular size or abnormal maxilla, a wide craniofacial base, and adenoid or tonsillar hypertrophy increases the risk of OSA.13 Smokers have a three–fold greater risk for OSA than non-smokers. The incidence

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of OSA during pregnancy in the first and third trimesters is 10.5 and 26.7 percent, respectively.14 Other medical conditions associated with OSA include congestive heart failure, acromegaly, hypothyroidism, chronic obstructive pulmonary disease (COPD), and end stage renal disease. One of the contributing factors for OSA with heart and renal failure is due to nocturnal rostral fluid shift. During sleep in the supine position, gravity moves fluid from the legs rostrally and increases fluid volume in the neck, increasing tissue pressure and collapsibility of the pharynx.15

Interaction of obesity and sleep disordered breathing Obesity is a major risk factor for SDB. An increase of 10% weight gain in patients with mild OSA can increase the severity of OSA by six fold. A 10% weight loss can result in a more than 20% improvement in OSA. Obesity causes pharyngeal airway narrowing by the enlargement of soft tissue structures within and surrounding the airway. Obesity also contributes to significant reduction of lung volumes by a combination of increased abdominal fat mass and supine position. The reduction of lung volume decreases longitudinal tracheal traction forces and pharyngeal wall tension, which causes narrowing of the airway. Hence, males with central or android obesity (apple shape) are more prone to have OSA than the gynecoid obesity (pear shape). Though OSA is not a component of metabolic syndrome (central obesity, hypertension, hyperlipidemia and insulin resistance), there are experimental and clinical evidence to show a relationship between OSA and increased cardiometabolic risk.16

Obesity hypoventilation syndrome OHS is a combination of obesity with body mass index (BMI) > 30 kg/m2, daytime hypercapnia with PaCO2 > 45 mmHg during wakefulness and absence of other alternative neuro5

muscular, mechanical, or metabolic explanation for hypoventilation. Although 90% of OHS patients have OSA, 10% do not. The prevalence of OHS is 0.15–0.6% of the general population and increases up to 50% with increase in BMI > 50 kg/m2.17 The prevalence of OHS in obese patients referred to sleep clinics is 9 to 20%17 and as high as 51% in obese patients with chronic hypoxemia.18 In contrast with OSA, a recent study in the Saudi population showed a higher prevalence of OHS in women (15.4%) versus men (4.5%) who were referred to sleep clinic.19 Compared to OSA patients, OHS patients have a restrictive respiratory pattern with increased work of breathing. As well, OHS patients have a blunted respiratory drive, in contrast with increased minute ventilation in obese patients with OSA. The increased level of leptin from adipose tissue in obesity is a respiratory stimulant, which helps to maintain eucapnia by increasing the minute ventilation in obese patients with OSA. But, there is a leptin resistance in OHS patents, which predispose them to hypoventilation. Most OHS patients are diagnosed after hypercapnic respiratory failure versus obese patients without hypercapnia, and they are more likely to have cardiorespiratory complications.20 Currently there is no criteria to grade the severity of OHS like OSA. A recent study has shown that the severity of the OHS can be determined by the PaCO2 level in the blood gas.21 The Malignant Obesity Hypoventilation Syndrome is a new terminology, a triad defined as a patient with a BMI > 40 kg/m2 with daytime hypercapnia, the metabolic syndrome and multi-organ dysfunction related to obesity.22

The overlap syndrome is a co-existence of OSA and COPD, a hypercapnic SDB. The incidence of daytime hypercapnia, respiratory failure and pulmonary hypertension is higher in the overlap syndrome patients than in isolated OSA or COPD. These patients present with hypoxemia and hypercapnic respiratory failure and are more difficult to treat than OHS.

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Perioperative risk of Obesity, OSA and OHS In the American College of Surgeons National Surgical Quality Improvement Program (ACS-NSQIP) database analysis of 16 major cardiovascular, orthopedic, and oncologic surgical outcomes, a BMI > 40 kg/m2 significantly increased the odds of venous thromboembolism, surgical site infection, acute kidney injury and cardiac complication with cardiac surgery.23 It did not show any increase in cardiopulmonary complications or mortality.23 The morbidly obese parturient is at increased risk for antenatal comorbidities, failed labor analgesia, longer first stage of labor and operative delivery.24 The Metabolic Syndrome is a risk factor for post-operative pulmonary complications, deep venous thrombosis, atrial fibrillation and congestive heart failure.25 A recent outcome study on the bariatric surgical population showed that pulmonary complications and metabolic syndrome were significantly associated with increased postoperative mortality.26

Though morbid obesity increases the perioperative risk, mild to moderately obese patients without comorbidities have a protective effect (Obesity Paradox) on the postoperative complications and cardiac morbidity.27,28 OSA has a significant impact on perioperative outcome.29 A recent review of 24 legal claims for perioperative complications due to OSA showed that 58% claims favored the plaintiff with an average financial compensation of 2.5 million dollars.30 More than half of the complications were related to anesthesia and the majority of them resulted in a vegetative state. OSA patients have a 2 times higher risk of pulmonary complications after non-cardiac surgery.31 In bariatric surgical patients, the presence of OSA was found to be an independent risk factor for adverse postoperative events. A meta-analysis showed

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that the presence of OSA increased the chances of postoperative cardiac events including myocardial infarction, cardiac arrest and arrhythmias (OR 2.1), respiratory failure (OR 2.4), desaturation (OR 2.3), intensive care unit (ICU) transfers (OR 2.8), and reintubations (OR 2.1).32 A recent meta-analysis showed that patients with STOP-Bang score 3 or greater are at higher risk of adverse post-operative events and longer length of stay.33 Ninety percent of patients with OHS were misdiagnosed and the 3-year mortality was worse than breast and colon cancer patients.34

Studies and meta-analysis suggest that patients with OSA, who have been managed with preoperative continuous positive airway pressure (CPAP), have fewer perioperative adverse events, especially cardio-pulmonary complications than those who are untreated.35,36,37,38,39 Though positive airway pressure therapy (PAP) is a “one size fits all” solution for most SDB, the goal is to relieve upper airway obstruction in OSA and increase the alveolar ventilation (i.e., PaCO2 <45 mmHg) in OHS. The two common modes of PAP therapy are CPAP and noninvasive ventilation (NIV). CPAP works by creating a positive pharyngeal transmural pressure and increasing the end-expiratory lung volume. The advantage of NIV over CPAP is that it augments the tidal volume with inspiratory pressure support. CPAP opens the airway obstruction of OSA and works in most OHS patients with OSA, but it may be inadequate to improve the alveolar ventilation in some. The most common type of NIV is Bi-level PAP (BPAP). This mode involves individual titration of inspiratory and expiratory PAP, the difference between these two settings correlates with the tidal volume. The average volume-assured pressure-support (AVAPS) ventilation is a newer mode of PAP therapy, which guarantees the delivery of a preset tidal volume with BPAP mode.

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Compared to OSA patients, surgical patients with OHS and overlap syndrome are more likely to experience prolonged intubation (OR, 3.1), postoperative heart failure (OR, 5.4), postoperative respiratory failure (OR, 10.9), postoperative ICU transfer (OR, 10.9), and longer hospital stay.20 Untreated OHS patients have higher mortality than treated OHS (23% vs 9%).40 Supplemental oxygen may be necessary for a group of OHS patients who desaturate even with PAP therapy.

Preoperative assessment Screening tests are imperative in this high-risk population.41, 42 Recent guidelines by the Society of Anesthesia and Sleep Medicine recommends routine OSA screening at pre-operative clinic for obese patients.6 Further preoperative testing should be individualized based on the comorbid conditions. Various screening tools like the Berlin questionnaire, STOP-Bang questionnaire and Epworth Sleepiness Scale are available.43 The STOP-Bang questionnaire has the highest validity and accuracy in predicting OSA in the perioperative setting.44,45 A STOPBang score of 5 - 8 identifies patients with a high probability of moderate-to-severe OSA46 (Table 1). The addition of serum HCO3- level ≥ 28 mmol/L to a STOP-Bang score ≥ 3 improves the specificity.47 Patients with a positive STOP-Bang score are more likely to have increased postoperative complications.33,48

The oxygen desaturation index from a high resolution nocturnal oximeter is a sensitive and specific screening tool to detect SDB in the surgical patients.49 Patients with mean overnight SpO2 < 93%, or oxygen desaturation index > 29 events/h were more likely to have postoperative adverse events.50 These screening tests are not helpful in distinguishing OSA from other sleep disorders, such as OHS and central sleep apnea. 9

If OHS is suspected, a blood gas analysis is the definitive test for identifying daytime hypercapnia in patients with OHS. Since it is an invasive test, other simple markers are an increase in serum bicarbonate level and low oxygen saturation. Increased serum HCO3- level due to metabolic compensation for chronic respiratory acidosis is common in OHS and other hypoventilation conditions. Recent data show an increase in serum bicarbonate without daytime hypercapnia can predict the early stage OHS among obese patients.51 The three clinical predictors of OHS are serum HCO3-, AHI, and lowest oxygen saturation during sleep. In addition, hypoxemia (SaO2 < 90%, corresponding to PaO2 < 60 mm Hg) during wakefulness should lead clinicians to suspect OHS in patients with OSA. A primary screening care pathway during the preoperative workup could identify the patients with SBD (Fig 1). Then suspected OHS patients can have a serum HCO3- as the initial test and polysomnography for the definite diagnosis. (Fig 2)

A modified STOP-Bang score with additional points for BMI (1 point for BMI ≥ 35–40 kg/m2, 2 points for BMI ≥ 40–45 kg/m2, 3 points for BMI ≥ 45 kg/m2) and HCO3- (1 point for bicarbonate ≥ 26–28 mmol/L, 2 points for bicarbonate ≥ 28 mmol/L) can increase the sensitivity for predicting OHS.

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Since the incidence of pulmonary hypertension is higher in OHS, simple

clinical signs to identify right heart failure such as evaluation for ankle edema and high jugular venous pressure is important. Though brain natriuretic peptide (BNP) measurement is not specific for right heart failure, it can be used to assess the level of severity and treatment effect in chronic hypercapnic respiratory failure.53

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Risk stratification The ASA physical status classification system is the most commonly used risk scoring system for surgical patients. Though the original scoring did not include obesity as a risk factor, BMI ≥ 40 kg/m2 is considered as ASA Status III in the recent update.54 The Obesity Surgery Mortality Risk Score is mainly used for patients undergoing gastric bypass, but it can be used for non-bariatric surgeries. This includes 5 risk factors: hypertension, BMI ≥ 50 kg/m2, male sex, ≥ 45 years, and known risk factors for pulmonary embolism (OHS, previous thromboembolism, preoperative vena cava filter, pulmonary hypertension).55 This risk score stratifies mortality risk into low (0 or 1 comorbidity), intermediate (2 to 3 comorbidities) and high (4 to 5 comorbidities) with mortality of 0.2%, 1.2%, and 2.4% respectively.55 However, obesity is not included in other commonly used surgical risk scoring systems like POSSUM (Physiological and Operative Severity Score for the enumeration of Mortality and Morbidity), SORT (Surgical Outcome Risk Tool) and NSQIP (National Surgical Quality Improvement Program) surgical risk calculator.56,57,58

Suitability for ambulatory surgery Based on the severity of sleep apnea, the type of anesthesia, invasiveness of surgery and the need of postoperative opioids, ASA has published guidelines on the perioperative management of OSA patients.4, The Society for Ambulatory Anesthesia (SAMBA) has endorsed a consensus statement on the preoperative selection of patients with OSA for ambulatory surgery.5 It recommends the STOP-Bang questionnaire as a screening tool for OSA. According to SAMBA guidelines, patients with a diagnosis of OSA with optimized comorbid conditions, compliant

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with CPAP, and minimal postoperative opioid requirements can be considered for ambulatory surgery (Fig. 3). Patients with moderate to severe OSA, who are noncompliant with CPAP may not be suitable for ambulatory surgery. At the same time, patients with a diagnosis of OSA based on the screening tool and optimized comorbid conditions may be considered for ambulatory surgery, if postoperative pain relief can be managed mainly with non-opioid analgesic techniques.

Currently there is no evidence on the optimal cut-off BMI for ambulatory surgery. A systematic review indicated that super-obese patients with BMI >50 kg/m2 are at increased risk for perioperative complications.59 Since patients with hypercapnic conditions like OHS are at higher risk for significant perioperative complications and more likely to have significant comorbid conditions, they may not be suitable for ambulatory surgery.

Perioperative infrastructure The health care team should have specific training in the issues relating to the care of morbidly obese patients. Patients should be encouraged to move themselves whenever possible during the perioperative care. The operating table, bed trolley and specific equipment such as the spine frame for spine surgery should be checked and labeled for its maximum limit on weight bearing capacity. For emergency surgeries, an “obesity pack” (including specific equipment, air assisted patient transfer system, protocol guidelines and contact numbers) should be readily available. The Society of Obesity and Bariatric Anesthesia (SOBA) has published a comprehensive one sheet guideline for managing the obese patients. (www.SOBAuk.com) The

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Italian Society of Anesthesia, Analgesia, Resuscitation and Intensive Care (SIAARTI) has recently published a consensus guideline on perioperative and periprocedural airway management and respiratory safety for the obese patient.60 Hospitals without intensive care facilities are not suitable for managing super morbid obese, OHS patients, and severe OSA patients noncompliant with CPAP.

Intraoperative management Obese patients present a different set of challenges and require specific perioperative care due to the possibility of difficult intubation, difficult mask ventilation, associated comorbidity, increased sensitivity to opioids, intraoperative and postoperative cardiorespiratory complications. SOBA has published guidelines on the perioperative care of obese patient.61 Induction of general anesthesia can precipitate a rapid fall in oxygen saturation, which can be minimized by a 25 degree head-up position during preoxygenation, the combination of preoxygenation with nasopharyngeal oxygen insufflation, and positive end-expiratory pressure (PEEP) of 10 cm H2O. Transnasal Humidified Rapid-Insufflation Ventilatory Exchange technique (THRIVE) is a promising new tool mainly used for apneic oxygenation and it can be used in obese patients for preventing desaturation with difficult airway management.62 The United Kingdom Fourth National Audit Project (NAP 4) reported a four fold increase in the risk of serious airway related complications in the morbidly obese patient.63 The incidence of difficult intubation in obese patients was twice as frequent in ICU than in the operating room and life-threatening complications related to airway management occurred 20-fold more often in ICU.64

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Positioning patients with TROOP or OXFORD pillow in the head elevated laryngoscopy position (“HELP”) facilitates direct laryngoscopy. A neck circumference greater than 42 cm and BMI more than 50  kg /m2 are associated with an increased risk of difficult intubation.65,66 The second generation double-lumen supraglottic airways, such as the LMA ProSealTM and the LMA SupremeTM, provide higher leak pressures and may be safer in patients with obesity.67 Securing the airway with an endotracheal tube would be a safer option for morbidly obese patients with gastric reflux disease or lithotomy position. Video laryngoscopic assisted intubation has a high success rate in the morbidly obese patients with a difficult airway.68 The use of awake video laryngoscopy-assisted tracheal intubation using topical local anesthesia of the airway has also been described as an alternate to flexible bronchoscopic intubation.69 According to the Difficult Airway Society guidelines,70 obesity and OSA are stratified into a category of ‘‘at risk’’ of a major complication during extubation. Reversal of neuromuscular block with sugammadex may reduce inadequate reversal of muscle relaxant in morbidly obese patients.71

The morbidly obese patients need protective ventilation with low tidal volumes (approximately 8 ml/kg) to avoid volutrauma and judicious use of oxygen to avoid absorption atelectasis.72,73 Recruitment maneuvers (PEEP & Valsalva) can counteract these effects. A recent meta-analysis shows that a recruitment maneuver added to PEEP compared with PEEP alone improves intraoperative oxygenation and compliance without adverse effects.74 Since morbidly obese patients are prone to postoperative hypoxemia due to atelectasis, patients should be extubated wide-awake in the sitting position if possible. Obese patients with OSA should have perioperative precautions and risk mitigation to achieve the best possible outcome (Table 2).

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Since obese patients are prone for DVT and rhabdomyolysis, careful positioning and precautions need to be taken with longer surgeries.

Regional anesthesia offers distinct advantages, which allows minimal airway manipulation, avoidance of anesthetic drugs with cardiopulmonary depression, reduced post-operative nausea and vomiting and reduced perioperative opioid requirements. However, the rate of block failure increased parallel with the level of obesity. Ultrasound-guided regional anesthesia for peripheral nerve blocks can improve the success rate in the obese population. Epidural analgesia can be utilized in obese patients undergoing laparotomy to improve postoperative respiratory function.75 Ultrasound guided neuraxial anesthesia is a viable option to increase the success in obese patients. 76 A recent study on more than 40,000 patients with OSA who underwent hip and knee arthroplasty, the use of neuraxial anesthesia vs. general anesthesia was associated with a reduction in need for mechanical ventilation, use of ICU, prolonged length of stay and cost.77

Postoperative management The morbidly obese patients with SDB who received general anesthesia should be observed for an additional 30-60 minutes in PACU after the modified Aldrete criteria for discharge has been met.

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(Fig. 4) The PACU team should be advised to look for recurrent

respiratory events (episodes of apnea ≥ 10 seconds, bradypnea <8 breaths/min, pain-sedation mismatch, or repeated O2 desaturation <90%).79 Any of the above events occurring repeatedly in separate 30-minute intervals should prompt the perioperative team for arranging a monitored bed or ICU care. Patients with suspected OSA and who develop recurrent PACU respiratory events

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are at increased risk of postoperative respiratory complications.79 These patients may require postoperative PAP therapy with postoperative monitoring.80 A recent trial has shown that postoperative oxygen therapy can improve the oxygenation and AHI in untreated OSA patients.81 However, 11.5% of these patients showed evidence of respiratory depression with elevated CO2. High concentrations of oxygen or providing oxygen alone without PAP to OHS patients should be avoided as this may worsen hypercapnia. Monitoring with continuous oximetry and/or capnography is recommended with parenteral opioids due to possible drug induced respiratory depression.82 Continuing PAP therapy in the postoperative period in the bariatric surgery patients may mitigate the risk of postoperative complications.83 An opioid-sparing multimodal analgesic package, including local anesthetic-infused nerve block catheters, wound catheters and nonopioid adjuncts (acetaminophen, nonsteroidal anti-inflammatory drugs), should be considered. If postoperative parenteral opioids are necessary, consideration should be made for the use of patient controlled analgesia with no background infusion and a strict hourly dose limit. Though patients with OSA are suitable for ambulatory surgery based on their level of optimization of comorbid conditions, patients with OHS or overlap syndrome who had general anesthetic and require postoperative opioids may not be suitable. There should be a team agreement in place regarding the post-operative pain prescription. Avoiding or minimizing opioid prescription for ambulatory surgery patients will prevent the worsening of obstructive episodes during the postoperative period.

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Conclusion Morbidly obese patients with sleep disordered breathing are at risk of perioperative morbidity. Identifying these high-risk patients and optimizing them with PAP therapy could reduce the risk significantly. The availability of care pathways is important to improve the outcomes of morbidly obese patients with or without SDB. Every perioperative team should have a written policy for managing these high-risk patients.

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Table 1 STOP-Bang Questionnaire Snoring? Do you Snore Loudly (loud enough to be heard through closed doors or your bedYes No partner elbows you for snoring at night)? Tired? Yes No Do you often feel Tired, Fatigued, or Sleepy during the daytime (such as falling asleep during driving)? Yes No Observed? Has anyone Observed you Stop Breathing or Choking/Gasping during your sleep? Yes No Pressure? Do you have or are being treated for High Blood Pressure? Yes No Body Mass Index more than 35 kg/m2? Yes No Age older than 50 year old? Neck size large? (Measured around Adams apple) Yes No For male, is your shirt collar 17 inches or larger? For female, is your shirt collar 16 inches or larger? Yes No Gender = Male? Scoring Criteria: For general population Low risk of OSA: Yes to 0-2 questions Intermediate risk of OSA: Yes to 3-4 questions High risk of OSA: Yes to 5-8 questions Yes to 2 of 4 STOP questions + individual’s gender is male Yes to 2 of 4 STOP questions + BMI > 35 kg/m2 Yes to 2 of 4 STOP questions + neck circumference male 17” Female 16” www.stopbang.ca Proprietary to University Health Network

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Table 2 Perioperative Precautions and Risk Mitigation for Patients with Sleep Disordered Breathing Anesthetic Concern Preoperative Screening SASM Guidelines6

Principles of Management  

 Ambulatory surgery criteria SAMBA Guideline5

Intraoperative Airway management (difficult mask ventilation and tracheal intubation)

  

OSA patients with optimized co-morbid conditions Patient using PAP therapy Postoperative pain mainly managed mainly with nonopioid analgesia



HELP positioning (Head Elevated Laryngoscopy Position) Pre-oxygenation with 25-degree head-up position & CPAP Nasal oxygen insufflation or THRIVE technique62 Anticipated difficult airway – Difficult airway equipment Rapid sequence induction with cricoid pressure for patients with GERD

 

 

Ventilation

OSA screening recommended to be a part of standard preanesthetic evaluation Additional evaluation for hypoventilation syndrome, severe pulmonary hypertension, and resting hypoxemia in the absence of other cardiopulmonary disease Continue PAP therapy, advise patients to bring PAP equipment to the surgical facility

      

Recruitment maneuver + PEEP to avoid atelectasis Protective ventilation - low TV & plateau pressure Second generation supraglottic device for better seal Minimize opioid use Use of short-acting agents (e.g. remifentanil) Multimodal approach to analgesia (NSAIDs, acetaminophen, tramadol, ketamine, gabapentin, pregabalin, dexmedetomidine, clonidine, dexamethasone) Consider local and regional anesthesia where appropriate

Extubation

 

Extubate wide-awake in the sitting position if possible Consider Sugammadex to prevent inadequate reversal

Monitored anesthetic care

 

Avoid deep sedation with unsecured airway Intraoperative capnography for monitoring of ventilation

Opioid-related respiratory depression

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Postoperative

  

Resume PAP therapy to avoid postoperative atelectasis Monitored bed for OSA patients with recurrent respiratory events, OHS and overlap syndrome patient Avoid long acting opioid prescription for ambulatory surgical patient

SASM: Society of Anesthesia and Sleep Medicine, PAP therapy: positive airway pressure therapy, SAMBA: Society for Ambulatory Anesthesia, CPAP: continous positive airway pressure. THRIVE: Transnasal Humidified Rapid-Insufflation Ventilatory Exchange. GERD: gastroesophageal reflux disease, PEEP: Positive end-expiratory pressure, TV: Tidal Volume, NSAIDs: Non-steroidal anti-inflammatory drugs, OSA: Obstructive sleep apnea, OHS: Obesity hypoventilation syndrome.

Raveendran R. Curr Opin Anaesthesiol. 2017;30:146-155.

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Figure 1: Screening algorithm for identifying patients with SBD

Subramani Y, et al. Sleep Med Clin. 2017;12:123-135.

21

Figure: 2 Perioperative management of the patient suspected to have OHS.

Chau EH, et al. Anesthesiology 2012; 117:188-205

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Figure 3: Decision making in preoperative selection of a patient with obstructive sleep apnea for ambulatory surgery

Adapted from SAMBA guideline Anesth Analg 2012; 115: 1060-8

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Figure 4 - Postoperative Management of the Diagnosed or Suspected OSA Patient after General Anesthesia.

Hillman DR et al. Respirology 2017; 22: 230–239

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