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 Table of Contents  
ORIGINAL ARTICLE
Year : 2019  |  Volume : 2  |  Issue : 3  |  Page : 135-141

Anaesthesiologists' role in diagnostic drug-induced sleep endoscopy and subsequent management strategy planning in obstructive sleep apnoea syndrome


Department of Anaesthesiology, JSS Academy of Higher Education and Research, Mysore, Karnataka, India

Date of Submission10-Dec-2019
Date of Acceptance13-Dec-2019
Date of Web Publication30-Jan-2020

Correspondence Address:
Dr. Nalini Kotekar
JSS Academy of Higher Education and Research, Mysore, Karnataka
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/ARWY.ARWY_35_19

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  Abstract 


Background and Aims: Obstructive sleep apnoea is characterised by repetitive partial or complete obstruction of the upper airway during sleep, leading to the reduction or cessation of airflow despite ongoing respiratory effort. Obesity, dyslipidaemia, hypertension, diabetes mellitus and cardiac arrhythmias are common co-existing comorbidities, placing patients at high risk for anaesthesia should they present for incidental or corrective surgeries. These patients are sensitive to opioids, induction and inhalational anaesthetics. Drug-induced sleep endoscopy (DISE) helps in assessing the exact site of airway obstruction and gives valuable inputs for surgical correction. The procedure includes stage-wise induction of sleep and airway visualisation during pharmacologically-induced sleep. Patients and Methods: Thirty patients, aged between 20 and 60 years, with a history of snoring and night arousals, were selected for DISE after taking informed consent. Intravenous propofol 0.5 mg/kg loading dose, followed by a titrated infusion of up to 50 μg/kg/min, was given throughout the procedure. The lowest value of oxygen saturation (SpO2), apnoeic episodes, total propofol used and DISE findings were documented. The airway was managed after the procedure till the patients regained full consciousness. Results: Lower SpO2 readings were observed in patients with complete collapse at the tongue base and in patients with floppy epiglottis. Conclusion: DISE is a dynamic, safe, easy-to-perform procedure that visualises the precise site of airway obstruction and guides in the planning of surgical correction thereafter. DISE findings provide valuable information for titrating doses of anaesthetic agents for incidental surgeries and perioperative management. However, the fine balance between identifying the obstruction and preventing desaturation is often challenging.

Keywords: Anaesthesiologists' role, drug-induced sleep endoscopy, obstructive sleep apnoea


How to cite this article:
Kukreja A, Shenkar A, Sathish K, Kotekar N. Anaesthesiologists' role in diagnostic drug-induced sleep endoscopy and subsequent management strategy planning in obstructive sleep apnoea syndrome. Airway 2019;2:135-41

How to cite this URL:
Kukreja A, Shenkar A, Sathish K, Kotekar N. Anaesthesiologists' role in diagnostic drug-induced sleep endoscopy and subsequent management strategy planning in obstructive sleep apnoea syndrome. Airway [serial online] 2019 [cited 2020 Apr 5];2:135-41. Available from: http://www.arwy.org/text.asp?2019/2/3/135/277330




  Introduction Top


The burden of obstructive sleep apnoea (OSA) on public health is comparable to that of smoking. OSA is the most prevalent sleep disordered breathing problem. It is characterised by repetitive partial or complete obstruction of the upper airway during sleep, leading to the reduction or cessation of airflow despite an ongoing respiratory effort. This results in repetitive episodes of hypoxia and carbon dioxide retention, provoking arousals to restore upper airway patency and consequently fragmenting sleep.[1] Patients with disordered breathing are at a high risk of disturbed breathing when sedated. Sedation is also deleterious for the protective mechanism of arousal. Upper airway abnormalities that predispose to obstructed breathing during sleep may also be the cause of difficult airway during intubation.

Between 9% and 26% of the middle-aged population is afflicted by OSA and is characterised by ≥15 obstructive events per hour of sleep or ≥5 obstructive events per hour of sleep and the presence of any related symptoms such as snoring, witnessed apnoea, nocturnal gasping or choking, excessive daytime sleepiness and non-restorative sleep.[2],[3] Most of these patients will have obesity, alterations in lipid profile, diabetes mellitus, hypertension and cardiac dysrhythmias, placing them in the high-risk category for anaesthesia. These patients are prone for exaggerated response to central nervous system depressants, inhalational anaesthetics and opioids.

In the general population, it is estimated that 4% of men and 2% of women meet the diagnostic criteria for OSA syndrome (OSAS).[4] Population-based epidemiologic studies have uncovered a high prevalence and a wide severity spectrum of undiagnosed OSA and have consistently found that even mild OSA is associated with significant morbidity. Severe OSA has a 5.2-fold greater risk for cardiovascular mortality and 3.8-fold greater risk for all-cause mortality than those without OSA.[4],[5]

The pathophysiological implications of OSAS can affect almost every organ in the body and thus have varied presentations to other medical specialties. Anaesthesiologists might encounter a patient with OSAS as a case of difficult intubation, increased sensitivity to opioids and other sedatives or with apnoeic episodes in the recovery period. These patients may present to the cardiologist with features of left ventricular hypertrophy, nocturnal angina, myocardial infarction, bradyarrhythmias, hypertension, heart failure or cor pulmonale. Psychiatrists are likely to encounter these patients presenting with symptoms of behavioural problems, depression, anxiety or acute delirium. On the other hand, these patients may present to the otorhinolaryngologist with snoring, sore throat or hoarseness for further treatment.[6]

The diagnosis and treatment of OSA is complex and multidimensional due to the difficulty in establishing the site of obstruction in awake patients of OSAS. Although screening questionnaires can be used for a preliminary assessment of OSA, their accuracy is limited. Polysomnography has been considered to be the standard diagnostic tool for OSA. It comprises of evaluation of the person's sleep pattern by using multiple parameters such as sleep cycle, sleep staging, oximetry, apnoeas/hypopnoeas and cardiac function. More than five obstructive apnoeas and hypopnoeas (Apnoea/Hypopnoea Index [AHI] >5 per hour), along with excessive daytime sleepiness or witnessed episodes of apnoeas and choking episodes at night, are sufficient to make the diagnosis of OSA.

Identification of the site of obstruction and pattern of upper airway changes during sleep are essential keys in guiding therapeutic approaches to OSAS. Croft and Pringle first proposed sleep endoscopy in 1991.[7] Using midazolam as a sedating agent, they demonstrated the utility of passing a fibreoptic endoscope through a sleeping patient's nasal cavity to assess pharyngeal structures for the evidence of obstruction and were able to induce preexisting snoring in 95% of their patients.[8] Drug-induced sleep endoscopy (DISE) is considered an integral part of the diagnostic workup in patients suspected with OSA being considered for corrective surgery. It is a safe and cost-effective tool to evaluate multiple levels of upper airway collapse during spontaneous ventilation while the patient is induced into pharmacologically produced unconscious sedation/simulated sleep. Studies have shown that DISE is a valid and reliable method to evaluate the site, degree and configuration of upper airway obstruction in adults with OSA.

A variety of sedative agents were used either alone or in combination for inducing and maintaining sleep during sleep endoscopy. Propofol is a commonly preferred hypnotic drug owing to its rapid onset, short half-life, easy titratability and ability to produce a similar state to non-rapid eye movements (NREM)sleep.[9] Propofol can be administered as small, repeated intravenous boluses, continuous intravenous infusion or target-controlled infusion (TCI). Moreover, its effect on respiratory depression is lower than that observed with benzodiazepines, and it leads to a low incidence of side effects (such as nausea or headache). It is also considered to be a very safe drug for sedation.[10] Propofol was preferred to dexmedetomidine in this study because the latter, when used as a sole sedative agent, may require high doses that may culminate in significant haemodynamic instability and delayed recovery.[11]

The most commonly used index to define the severity of OSA is the AHI, calculated as the number of obstructive events per hour of sleep and obtained by nocturnal cardiorespiratory monitoring. The American Academy of Sleep Medicine has classified OSA into mild, moderate and severe OSA.

Mild OSA

AHI of 5-15 per hour; involuntary sleepiness during activities that require little attention, such as watching television or reading.

Moderate OSA

AHI of 15-30 per hour; involuntary sleepiness during activities that require some attention, such as meetings or presentations.

Severe OSA

AHI of more than 30 per hour; involuntary sleepiness during activities that require more active attention, such as talking or driving.

Advances in sleep medicine and the availability of improved diagnostic tools have led to a better recognition and treatment of the disease. The management of patients with OSA requires a multidisciplinary approach and many treatment options are currently available.

The non-surgical treatment options currently available include positive airway pressure and oral appliances such as tongue-retracting devices and mandibular advancement devices. Continuous positive airway pressure (CPAP) is considered the gold standard in the treatment of OSA as it acts as a pneumatic splint and stabilises the upper airway. Bi-level positive airway pressure (Bi-PAP) is used to administer varying pressures between the inspiratory and expiratory cycles. Bi-PAP is considered for patients with intolerance to CPAP or patients with hypoventilation due to obesity or neuromuscular disease. Mandibular advancement devices are indicated in cases who are non-compliant for CPAP and patients with a good dentition and body mass index (BMI) <30 kg/m 2. Surgical options include correction of nasal, palatal, maxillary and mandibular defects.[3]


  Patients and Methods Top


Patients scheduled for DISE from the Department of Otorhinolaryngology were included in this prospective clinical study. Thirty patients between 20 and 60 years with OSAS who fulfilled the inclusion criteria after undergoing polysomnography were selected. Patients unwilling to participate and those with acute respiratory tract infections or uncontrolled systemic disorders such as diabetes or cardiac arrhythmias were excluded from the study.

Procedure of drug-induced sleep endoscopy

After performing a thorough preoperative evaluation and obtaining informed consent, the patients were kept nil by mouth for 6 hours prior to the procedure. All equipment for difficult intubation were kept ready. All sleep endoscopies were carried out in an operation theatre setting. Patients were placed in the supine position in comfortable ambient temperatures. An intravenous line was secured with an 18 SWG cannula, and the patients were premedicated with intravenous ondansetron 0.1 mg/kg and glycopyrrolate 0.2 mg. Supplemental oxygen was provided with nasal catheter at 2 L/min. Sleep was induced with a bolus dose of 0.5 mg/kg of propofol and maintained with a titrated infusion of propofol up to a maximum of 50 μg/kg/min till the procedure got over. The same otorhinolaryngologist performed the procedure using flexible nasopharyngoscope in all the patients studied. No topical anaesthesia was used. The nasal endoscope was passed via the naris after the initial bolus of propofol. The patients were monitored till they regained complete consciousness. With the endoscope in position to observe the velopharynx, the sedation sequence proceeded until the onset of obstruction was noted. This was identified as the obstruction clinical end point. The pharynx was observed, and images of the anatomic sites of obstruction were obtained. The infusion was then terminated and the patient was allowed to wake up.

Parameters studied

Lowest oxygen saturation (SpO2), number of apnoeic episodes, site of airway obstruction, complete or partial obstruction, direction of obstruction (anteroposterior or lateral), need for intubation and total requirement of propofol were studied during the procedure. Descriptive statistics were used to summarise the data by measuring the mean, median, standard deviation and proportions. Inferential statistics were assessed using Chi-square test, ANOVA, correlation and Kruskal–Wallis test. P < 0.05 was considered statistically significant. While SPSS statistics software Version 21.0 for Windows (IBM Corp., Armonk, NY, USA) was used for statistical analysis, graphs were created using Microsoft Excel.


  Results Top


Of the thirty patients in our study, 43.4% belonged to the age group of 31-40 years, 40% belonged to the age group of 41-50 years and 16.6% belonged to the age group of 21-30 years [Table 1]. The mean age was 37.3 ± 7.2 years. In this study population, 90% were males and 10% were females [Table 1]. We observed that 63.3% of the patient population fell into the category of overweight, 20% were obese and 16.7% were normal. The mean BMI of the patient population was 27.71 ± 2.38 kg/m 2 [Table 2].
Table 1: Age and gender distribution of patients

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Table 2: Body mass index of patients

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The mean of the lowest SpO2 recorded was 87.8% ± 5.07% in 21-30 years, 84.54% ± 6.08% in 31-40 years and 75.33% ± 9.47% in 41-50 years [Table 3]. Comparison of BMI and SpO2 revealed the mean lowest SpO2 to be 90.2% ± 2.77% in normal patients, 83.05% ± 5.14% in overweight patients and 68.83% ± 9.11% in obese patients [Table 4].
Table 3: Oxygen saturation of patients (oxygen saturation) grouped by age

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Table 4: Relationship of oxygen saturation to body mass index

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The most common cause of OSA was noted to be partial airway obstruction at the tongue base (40.0%), followed by retropalatal obstruction (23.3%) [Table 5]. The lowest SpO2 was seen in cases with complete airway obstruction with floppy epiglottis (SpO258%) followed by complete airway obstruction at tongue base (SpO274%). Eight percent of the patients in the age group of 21-30 years had no apnoeic episodes, whereas 20% had 1-3 apnoeic episodes. In the age group of 31-40 years, 69.2% of the patients had no apnoeic episodes, 15.4% had 1-3 apnoeic episodes and a further 15.4% had 4-6 apnoeic episodes. In the age group of 41-50 years, 41.7% of the patients had no apnoeic episodes, 25% had 1-3 apnoeic episodes and 33.3% had 4-6 apnoeic episodes [Table 6].
Table 5: Anatomical abnormality resulting in obstructed breathing

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Table 6: Details of number of apnoeic episodes linked to age

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We noted that while 80% of the patients with normal BMI and 73.7% of the overweight patients did not have any apnoeic episodes, all the six obese patients had apnoeic episodes. Among these six obese patients, two had 1-3 apnoeic episodes, whereas the remaining four had 4-6 apnoeic episodes [Table 7].
Table 7: Details of number of apnoeic episodes related to body mass index

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Statistically significant correlation existed between age and lowest SpO2(P = 0.001) and BMI and lowest SpO2(P = 0.0001). We also noted a statistically significant correlation between age (P = 0.058) and BMI (P = 0.0001) on total propofol requirement [Table 8].
Table 8: Relationship of oxygen saturation and total propofol dose to age and body mass index

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  Discussion Top


DISE provides a real-time, dynamic assessment of the patterns of obstruction during sleep, albeit pharmacologically induced. This is a niche procedure where the anaesthesiologist is required to perform the anaesthesia within a narrow range of anaesthetic depth. The DISE-naive anaesthesiologist is likely to have limited experience with the graded titration of propofol to the specific end point of airway obstruction without inadvertently creating airway obstruction needing airway intervention. The 'ideal' drug for DISE should have a short half-life and should be compatible for use as an intravenous bolus and infusion. It should have the least impact on respiratory drive, muscle tone and REM sleep. Propofol, the current drug of choice, can be administered via manual infusion or TCI.

The effect of sedation on the anatomical pattern of obstruction may be different. Rabelo et al. reported that the use of propofol reduced REM-sleep, which altered the sleep architecture slightly, but did not influence the respiratory pattern, nor significantly influence the AHI.[12] Excessive sedation is associated with decrease of upper airway muscle tone and increases in pharyngeal critical closing pressures. Various articles have described respective sedation methods, but there is no standardised protocol.[13] The ideal concentrations differ per individual, depending on his or her susceptibility to the sedative effects of the drug. Slow, stepwise induction is vital to avoid oversedation which might lead to false-positive results.

All patients were monitored for noninvasive blood pressure, oxygen saturation, respiratory rate and electrocardiography. Ideally, the evaluation of the level of consciousness can be done with the bispectral index (BIS). Loss of consciousness has been reported at BIS values between 60 and 80.[14] Moreover, different BIS levels have shown varied degrees of upper airway obstruction.

DISE poses various challenges to the anaesthesiologist such as hypotension, bradycardia, arrhythmias, laryngospasm, gag reflex, apnoea or aspiration. Bradycardia, diagnosed when heart rate dropped <60/min, was treated with atropine 0.01 mg/kg. Hypotension was diagnosed if the mean arterial pressure dropped below 70% of the baseline and treated with intravenous crystalloids. Fall in saturation was treated with supplemental oxygen of 4–6 L/min, jaw thrust and chin lift. Ventilation with facemask and 100% oxygen was provided in case of persistent desaturation.

The DISE findings were recorded according to obstruction at various levels in the upper airway. Airway collapse due to floppy epiglottis [Figure 1] and circumferential collapse of the airway [Figure 2] were the two examples of anatomical abnormalities causing airway obstruction. The severity of obstruction was graded using the VOTE classification (velum/oropharynx/tongue base/epiglottis) and recorded as patent, partial obstruction or complete obstruction. Partial obstruction was defined as a decrease in the lumen to <70% of the expiratory status and complete obstruction was recorded when no lumen was visible.[15] Multiple level obstruction was recorded when there was obstruction at two or more sites.
Figure 1: Airway collapse due to floppy epiglottis

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Figure 2: Circumferential collapse of the airway

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It is pertinent to understand that the upper airway is not restricted to two independent regions (palate and hypopharynx), each containing various structures that can contribute to significant airway obstruction in isolation. Instead these two regions, along with associated structures, have dynamic interactions that are not completely understood. As surgical procedures are directed at specific structures, DISE may improve procedure selection and outcomes. The three structures that most commonly cause hypopharyngeal airway obstruction are the tongue, epiglottis and the lateral pharyngeal walls.[16] The corrective techniques on the hypopharyngeal airway, surgical and nonsurgical, may exert differential effects on these various structures. A diagnostic test has value in terms of helping determine whether hypopharyngeal obstruction is present and which structure is implicated most in that obstruction.

A major risk factor for surgical failure in patients undergoing single level surgery such as uvulopalatopharyngoplasty (UPPP) is the presence of severe retrolingual collapse.[17] It is therefore very critical that the preoperative airway evaluation of patients with OSA reflects the actual severity of airway collapse present during sleep, as against that seen on awake endoscopic procedures that examine static physical attributes that fail to account for upper airway muscle relaxation known to occur during sleep.

This study is not without limitations. First, as the study population was small, it could be labelled a biased sample, as it did not mirror the general OSA population. Second and, ideally, sleep endoscopy should be performed during natural sleep. This is a tedious and challenging procedure and is therefore rarely used. Other potential limitations of this study include the rating of DISE findings by a single observer; the confounding effect of degree of sedation on DISE findings; the classification of severity of OSA and small number of patients in mild OSA group. The degree of sedation has a confounding effect on DISE findings as excessive sedation decreases upper airway muscle tone and increases pharyngeal critical closing pressure.

As DISE findings were assessed subjectively, the evaluation of findings by a single observer potentially leads to biased findings, therefore DISE findings were evaluated by a blinded observer who did not know the severity of OSA. We did not evaluate the interrater reliability of the findings; however, interrater reliability of DISE is reported to be moderate to substantial.

Standardising the method of sedation, identification of a uniform DISE classification system and definition of a reproducible and titratable standard mandibular advancement manoeuvre continue to remain the future challenges for DISE. Future research should focus on these topics to increase the already well-recognised role of DISE. Our data suggest that DISE is safe, is easy to perform, is valid and is reliable, as has been previously reported. Furthermore, we found a good correlation between DISE findings and clinical characteristics, which is in agreement with the existing literature.


  Conclusion Top


Sleep-disordered breathing is a highly prevalent problem among all age groups, particularly in association with significant comorbidity. The perioperative management of these patients is affected by the pathological consequences of the disease. Anaesthesiologists are likely to screen large patient populations with obstructive sleep apnoea, a source of significant community morbidity. Sleep endoscopy is a remarkable diagnostic tool for dynamic assessment of the airway in a sleeping patient with OSAS. Such assessment assists the surgeon to tailor the treatment plan for each patient based on the level and pattern of airway obstruction. Planning a management strategy based on the findings of DISE not only improves the results of surgical intervention but also minimises the scope of intervention. DISE is integrated with the VOTE classification, an easily applicable grading system. While a multilevel collapse and tongue base collapse are associated with higher AHI values, a tongue base collapse or epiglottis collapse is associated with positional OSA. A complete concentric collapse is associated with an increased BMI and a raised BMI is associated with a decreased success rate. A complete assessment of all sites of obstruction with use of both DISE and VOTE classification targets treatment success of OSA.

Acknowledgement

We acknowledge the contribution of Professor M Bharathi, Head of Department of Otorhinolaryngology, JSS Academy of Higher Education and Research, Mysore, Karnataka, India.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
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Marin JM, Carrizo SJ, Vicente E, Agusti AG. Longterm cardiovascular outcomes in men with obstructive sleep apnoea-hypopnoea with or without treatment with continuous positive airway pressure: An observational study. Lancet 2005;365:1046-53.  Back to cited text no. 4
    
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Marshall NS, Wong KK, Liu PY, Cullen SR, Knuiman MW, Grunstein RR. Sleep apnea as an independent risk factor for all-cause mortality: The Busselton Health Study. Sleep 2008;31:1079-85.  Back to cited text no. 5
    
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Kotani Y, Shimazawa M, Yoshimura S, Iwama T, Hara H. The experimental and clinical pharmacology of propofol, an anesthetic agent with neuroprotective properties. CNS Neurosci Ther 2008;14:95-106.  Back to cited text no. 9
    
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Petroz GC, Sikich N, James M, van Dyk H, Shafer SL, Schily M, et al. A phase I, two-center study of the pharmacokinetics and pharmacodynamics of dexmedetomidine in children. Anesthesiology 2006;105:1098-110.  Back to cited text no. 11
    
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Rabelo FA, Braga A, Küpper DS, De Oliveira JA, Lopes FM, de Lima Mattos PL, et al. Propofol-induced sleep: Polysomnographic evaluation of patients with obstructive sleep apnea and controls. Otolaryngol Head Neck Surg 2010;142:218-24.  Back to cited text no. 12
    
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Abdelgalel EF. Dexmedetomidine added to propofol for drug-induced sleep endoscopy in adult patients with obstructive sleep apnea: Randomized controlled trial. Egyptian J Anaesth 2018;34:151-7.  Back to cited text no. 13
    
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Whitlock EL, Villafranca AJ, Lin N, Palanca BJ, Jacobsohn E, Finkel KJ, et al. Relationship between bispectral index values and volatile anesthetic concentrations during the maintenance phase of anesthesia in the B-Unaware trial. Anesthesiology 2011;115:1209-18.  Back to cited text no. 14
    
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Lo YL, Ni YL, Wang TY, Lin TY, Li HY, White DP, et al. Bispectral index in evaluating effects of sedation depth on druginduced sleep endoscopy. J Clin Sleep Med 2015;11:1011-20.  Back to cited text no. 15
    
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Soares D, Folbe AJ, Yoo G, Badr MS, Rowley JA, Lin HS. Drug-induced sleep endoscopy vs awake Müller's maneuver in the diagnosis of severe upper airway obstruction. Otolaryngol Head Neck Surg 2013;148:151-6.  Back to cited text no. 17
    


    Figures

  [Figure 1], [Figure 2]
 
 
    Tables

  [Table 1], [Table 2], [Table 3], [Table 4], [Table 5], [Table 6], [Table 7], [Table 8]



 

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