Toll Free: 855.244.7533 | F: 855.201.3647
Home Sleep Testing Monitor
In 1993, Croft and Pringle developed a grading scale that utilized sleep endoscopy to categorize snoring and obstruction. Grading was based on whether the obstruction was palatal, multilevel, or tongue-based.[2] Sleep endoscopy, in combination with the grading scale, allows the physician to directly observe pharyngeal structures in the sedated patient with OSA and categorize the obstruction.
Another grading system that uses sleep endoscopy to assess airway obstruction utilizes 3 separate evaluations of the pharynx. The first analysis uses a dichotomous assessment to identify individual areas of obstruction in the palate and hypopharynx regions. The second analysis assesses the percentage of obstruction in each area: less than 50%, 50-75%, and more than 75%, representing mild, moderate, and severe obstruction, respectively.
Based on the level and pattern of airway obstruction in a patient with OSA, sleep endoscopy allows the physician to tailor the treatment plan to each patient. This can improve the results of surgical intervention and/or minimize the scope of intervention. Sleep endoscopy may also provide information that erases the need for surgery altogether.
For example, nearly 70% of patients surveyed in an outpatient setting by Hewitt et al were determined to have a palatal cause of obstruction and were prescribed surgical intervention. However, after the patients underwent sleep endoscopy, that figure dropped to 54%, reducing the number of procedures performed.
The high success rate of customized treatment for OSA has been attributed to the targeted selection offered by sleep endoscopy.[5] The multimedia clip below shows typical findings seen on routine DISE.
Other techniques for OSA assessment
Otolaryngologists use numerous modalities to locate the site of snore-sound generation and obstructive locations. These tools include a complete head-and-neck exam, the Müller maneuver, lateral radiographic cephalometry, computed tomography (CT) scanning, and magnetic resonance imaging (MRI). The static nature of these exams, coupled with increased resting muscle tone while the patient is awake, makes pinpointing the source of true obstruction difficult. While each of these methods offers reasonable diagnostic efficacy, none offers direct and dynamic visualization of pharyngeal structures during sleep.
Indications and Contraindications
Any patient who has documented OSA and is a potential candidate for OSA surgery should be considered for DISE via propofol. This dynamic exam will study the patient’s real-time OSA under light sedation, complementing the complete head-and-neck exam and (utilizing the Müller maneuver) awake endoscopy.
The ideal patient should have:
Documented OSA
An airway deemed manageable by the anesthesiologist and the operating surgeon
A patent nasal airway and nasopharynx, to allow the fiberoptic scope to pass unimpeded
Absolute contraindications include patients who are pregnant or who have a known history of propofol allergy. Other contraindications are significant nasal obstruction that impedes passage of the flexible fiberoptic laryngoscope (FFL), an “unsafe” airway, a frank aspiration history, and allergies to propofol components such as egg lecithin or soybean oil.
Outcomes
Due to the subjective nature of evaluating airway collapse during sedation, the question of sleep endoscopy’s reliability is a concern.
When comparing assessments by 2 independent reviewers of prerecorded sleep endoscopy procedures, Kezirian et al demonstrated moderate to substantial interrater reliability. This was significant in the identification of primary structures involved in obstruction versus individual structures.
This same study demonstrated a higher interrater reliability for assessment of the palatal region for obstruction in general versus assessment of individual structures that cause obstruction in the palatal region. The authors stated that the lower reliability in assessing individual structures is less important in palatal obstruction, because traditional uvulopalatopharyngoplasty (UPPP) treatment is the same regardless of the structure involved, be it the soft palate or velopharynx lateral pharyngeal wall.
(However, there has been developing interest in UPPP modifications. These include the expansion pharyngoplasty, uvulopalatal flap,anterior palatoplasty, and Z-palatopharyngoplasty. Each of these modifies the palate in various ways, creating either a superior and lateral pull, an anterior pull, or a combination pull on the palate and pharynx. Application of these specific palate procedures based on DISE could change how the palate is addressed.)
Kezirian et al's study also mentions that the tongue, epiglottis and lateral pharyngeal walls are the 3 structures most commonly involved in obstruction in the hypopharynx. At this site, there is a moderate to substantial interrater reliability in assessing individual hypopharyngeal structures that cause obstruction. Because there are varying treatment options for the different structures that are involved, sleep endoscopy can help to determine which hypopharyngeal and oropharyngeal procedure will be the most efficacious.
A study by Rodriguez-Bruno et al concluded that sleep endoscopy has good reliability, particularly in the evaluation of hypopharyngeal structures. The investigators looked at test-retest reliability, comparing the results from 2 distinct exams analyzed by 1 person. When retrospectively reviewing more than 2,400 procedures involving patients with symptoms of sleep-disordered breathing, Kotecha et al demonstrated greater than 98 percent effectiveness of sleep endoscopy in producing snoring in patients. This conclusion was important, because in order for sleep endoscopy to be a valid tool for evaluating obstruction, it has to be proficient in recreating sleeplike conditions.
Concerns regarding the potential for false-positives with sedation revolve around the premise that sedation-induced sleep can cause a greater degree of muscle relaxation than physiologically natural sleep does. Critics argue that snoring may be induced in the patient who otherwise would not exhibit symptoms during normal sleep.
However, when nonsnorers who underwent similar sedation techniques were compared with individuals with self-described snoring problems, the nonsnorers were not induced to snore with sedation.
Another concern with sleep endoscopy is whether or not the sedation-induced sleep alters the sleep profile. Rabelo et al showed that patients induced with propofol did not enter rapid eye movement (REM) sleep during sedation and that these patients tended to remain in slow-wave sleep. When the apnea-hypopnea indexes (AHIs) between propofol-induced patients and those whom slept without sedation were compared, there was little difference between the groups. Although the fundamental sleep architecture is changed in a patient with OSA, propofol has been shown to not change the respiratory pattern in patients with apnea;
Another study demonstrated a reduction in the duration of REM sleep in patients undergoing DISE; however non-REM sleep patterns were unchanged.[16] It is important to note that, although it is believed that the majority of apneic events occur during REM sleep, research has shown that AHIs measured during REM and non-REM sleep in patients with OSA do not differ significantly.
Intraprocedural grading using any of the methods described above typically correlates well with results of AHI, and it has been shown that AHIs measured after targeted therapy directed by sleep endoscopy are significantly lower.
In a study comparing 207 primary snorers without OSA with 117 subjects with OSA after receiving sedation, a higher degree of collapsibility was seen in the OSA group, with a correlation observed between the AHI during natural sleep and the degree of hypopharyngeal obstruction during sleep endoscopy.
Complications in sleep endoscopy
Complications associated with sleep endoscopy include the following:
Epistaxis from the flexible laryngoscope
Laryngospasm
Aspiration
Loss of the airway
Need for a surgical airway
Applications of Sleep Endoscopy
The following are examples of various uvulopalatopharyngoplasty and hypopharyngeal modifications for select dynamic airway findings seen on DISE:
Lateral collapse of the oropharyngeal airway - Expansion sphincter palatopharyngoplasty (Tucker/Pang source)
Oropharyngeal anterior-to-posterior collapse - Uvulopalatal flap, anterior palatoplasty
Oropharyngeal concentric collapse - Combination of lateral and anterior-to-posterior collapse techniques, Z-palatopharyngoplasty
Hypopharyngeal base of tongue collapse - Submucosal minimally invasive lingual excision (SMILE), radiofrequency ablation of the base of tongue
Epiglottic collapse - Hyoid suspension (this also helps with lateral hypopharyngeal collapse)
Sleep endoscopy is a great tool for teaching others about airway management, and it is helpful for anesthesiology and otolaryngology residents who are learning about airway anatomy and physiology.
Relevant Anatomy
The pharynx is bounded by the base of the skull superiorly; the cricoid cartilage inferiorly; and the nasal cavities, the oropharyngeal inlet, and the base of the tongue anteriorly.
The boundaries of the oropharynx are the lower edge of the soft palate superiorly and the hyoid bone inferiorly. The anterior border is formed by the oropharyngeal inlet and the base of the tongue, and the posterior border is formed by the superior and middle pharyngeal constrictor muscles and their overlying mucosa.
Inferiorly, the posterior one third of the tongue, or the base of the tongue, continues the anterior border of the oropharynx. The vallecula, which is the space between the base of the tongue and the epiglottis, forms the inferior border of the oropharynx. This is typically at the level of the hyoid bone.
The borders of the hypopharynx are the hyoid bone superiorly and the upper esophageal sphincter (UES), or cricopharyngeus muscle, inferiorly.
The anterior boundary of the hypopharynx consists largely of the laryngeal inlet, which includes the epiglottis and the paired aryepiglottic folds and arytenoid cartilages. The posterior surface of the arytenoid cartilages and the posterior plate of the cricoid cartilage complete the anteroinferior border of the hypopharynx. Lateral to the arytenoid cartilages, the hypopharynx consists of the paired piriform sinuses, which are bounded laterally by the thyroid cartilage.
April 12, 2010 -- NEW YORK (Reuters Health), Apr 12 - Patients who snore under conscious sedation during colonoscopy probably have obstructive sleep apnea (OSA), researchers from Lebanon suggest.
Out of 20 sedated patients who snored during colonoscopy in their study, all turned out to have sleep apnea. Conscious sedation can alter the normal respiratory response to hypoxemia and hypercapnia and facilitate pharyngeal collapse in patients with OSA, according to Dr. Ala I. Sharara and colleagues -- so endoscopy may therefore provide "a unique opportunity" to make a diagnosis that might otherwise be missed. For the study reported online March 22 in Gastrointestinal Endoscopy, Dr. Sharara and colleagues at the American University of Beirut Medical Center recruited 131 patients who were undergoing outpatient colonoscopy. They found that 24 (18%) snored continuously for 10 seconds or longer during conscious sedation with meperidine and midazolam. All were lying in the left lateral decubitus position. Twenty of the snorers and 18 controls matched by age and body mass index underwent portable home polysomnography. All 20 snorers and four controls had OSA, for a positive predictive value of 100% and a negative predictive value of 78%. Fourteen snorers and one control had moderate or severe OSA (p < 0.001; positive predictive value 70%, negative predictive value 94%). The authors had also performed physical exams and assessed sleepiness using validated tools. But snoring during conscious sedation was superior to any other indicators for predicting OSA. In fact, it was the only independent predictor of OSA on multivariate analysis (odds ratio 33.3). "Given the medical and financial burden of undiagnosed OSA, these patients should be carefully identified and referred for sleep medication evaluation," Dr. Sharara and associates conclude. The researchers acknowledge the limitations of their study, including its small sample size and lack of capnographic monitoring. Also, they point out, detecting OSA during endoscopy depends on the vigilance of the endoscopy team and may be affected by the type of sedatives used, depth of sedation, and patient positioning. Gastrointest Endosc 2010. |
Out of 20 sedated patients who snored during colonoscopy in their study, all turned out to have sleep apnea. Conscious sedation can alter the normal respiratory response to hypoxemia and hypercapnia and facilitate pharyngeal collapse in patients with OSA, according to Dr. Ala I. Sharara and colleagues -- so endoscopy may therefore provide "a unique opportunity" to make a diagnosis that might otherwise be missed. For the study reported online March 22 in Gastrointestinal Endoscopy, Dr. Sharara and colleagues at the American University of Beirut Medical Center recruited 131 patients who were undergoing outpatient colonoscopy. They found that 24 (18%) snored continuously for 10 seconds or longer during conscious sedation with meperidine and midazolam. All were lying in the left lateral decubitus position. Twenty of the snorers and 18 controls matched by age and body mass index underwent portable home polysomnography. All 20 snorers and four controls had OSA, for a positive predictive value of 100% and a negative predictive value of 78%. Fourteen snorers and one control had moderate or severe OSA (p < 0.001; positive predictive value 70%, negative predictive value 94%). The authors had also performed physical exams and assessed sleepiness using validated tools. But snoring during conscious sedation was superior to any other indicators for predicting OSA. In fact, it was the only independent predictor of OSA on multivariate analysis (odds ratio 33.3). "Given the medical and financial burden of undiagnosed OSA, these patients should be carefully identified and referred for sleep medication evaluation," Dr. Sharara and associates conclude. The researchers acknowledge the limitations of their study, including its small sample size and lack of capnographic monitoring. Also, they point out, detecting OSA during endoscopy depends on the vigilance of the endoscopy team and may be affected by the type of sedatives used, depth of sedation, and patient positioning. Gastrointest Endosc 2010. |
apnea-hypopnea index in patients with gastroesophageal reflux disease and obstructive sleep apnea
Pál Demeter, Katalin Várdi Visy, Pál Magyar
INTRODUCTION
There is an increasing mass of evidence for a link between the obstructive sleep apnea (OSA) and gastroesophageal reflux disease (GERD). The large negative intrapleural pressure swings during apnea should facilitate reflux events[1]. A further factor to be considered regarding the OSA-GERD relationship is that the diaphragm is connected to lower esophageal sphincter (LES) through the phreno-esophageal ligament (PEL). During apnea the respiratory work of the diaphragm increases extremely. This increased burden affects the cardia through the frequent change of the position of PEL. This leads partly to the loss of the cardia muscle tone[2]. The European Community Respiratory Health Survey published in 2002 noted that GERD development during sleep is an important determinant of the respiratory balance, since it may play a role as an aggravating or causal factor in relation to the nocturnal asthma, chronic cough, recurrent bronchitis and respiratory disorders during sleep[3]. A higher frequency of GER-related symptoms has been found in patients with OSA than in the control subjects[4,5]. More reflux events could be identified in OSA patients than in controls during one-channel esophageal pH-metry[6]. The number of reflux events could be reduced with nasal continuous positive airway pressure (nCPAP) treatment for both the patients with OSA and GERD[7-9]. These data suggest that OSA may be a significant cause of GERD.
The influence of the severity of OSA on endoscopic findings in patients with GERD and OSA has not been analyzed yet.
MATERIALS AND METHODS
Fifty-five patients with proven OSA were referred for upper panendoscopy. Diagnosis of sleep apnea was based on a 12-channel polysomnography (2-channel EEG/ electroencephalography/, EOG/electrooculography/, chin EMG/electromyography/, ECG/electrocardiography/, nasal and oral flow-metry, detection for O2-saturation, pulseoxymetry, detection for thoracic and abdominal movements, phonometry) performed using the Morpheus Medatech system in our sleep lab. All patients underwent upper panendoscopy and were asked about the frequency of typical reflux symptoms. Epworth sleepiness scale (ESS)[10] was completed by patients to measure their daytime sleepiness.
AIM: To assess the relationship between severity of gastroesophageal reflux disease and apnea-hypopnea index (AHI) as an indicator of the severity of obstructive sleep apnea.
METHODS: Data of 57 patients with proven obstructive sleep apnea and gastroesophageal reflux disease were analyzed. Patients were divided into two groups according to severity of the sleep apnea:
“mild-moderate” (A)-AHI 5-30,
n = 27, “severe” (B)-AHI >30,
n = 30.
All patients underwent apnea monitoring during the night, upper panendoscopy and were asked about typical reflux symptoms.
RESULTS: All examined patients in both groups showed a significant overweight and there was a positive correlation between body mass index and the degree of sleep apnea (P = 0.0002). The occurence of erosive reflux disease was significantly higher in “severe” group (P = 0.0001). Using a logistic regression analysis a positive correlation was found between the endoscopic severity of reflux disease and the AHI (P = 0.016). Forty-nine point five percent of the patients experienced the typical symptoms of reflux disease at least three times a week and there was no significant difference between the two groups.
CONCLUSION: A positive correlation can be found between the severity of gastroesophageal reflux disease and obstructive sleep apnea.
© 2005 The WJG Press and Elsevier Inc. All rights reserved.
The classification of GERD was based on endoscopic findings. We used the conventional Savary-Miller classification of the disease[11]. The patiets’ data were collated on an Excel 9.0 worksheet, including the severity grades of GERD (0-4), the apnea-hypopnea index (AHI), the frequency of typical GERD symptoms (heartburn, regurgitation of gastric content, dysphagia, age, gender, the score of ESS and body mass index /BMI/. The patients were divided into two groups according to the severity of sleep apnea[12] :
“mild-moderate” (A)-AHI 5-30, n = 27;
“severe” (B)-AHI >30, n = 30
Statistical analysis
In case of continuous and category variables, a nonparametric t test (Mann-Whitney), one way ANOVA test and χ2 test were used. In the event of dichotomous variables, χ2 “for trend” test was performed. The relationship between the severity of reflux disease and AHI was analyzed with the help of logistic regression analysis.
We relied on the conventional P<0.05 critical values regarding the statistical tests of the results. We used the SPSS 9 for Windows software package for the statistical procedures.
RESULTS
The total available population covered 57 patients. This population was characterized by an
average age of 51.38 years (SD±9.16), a male/female ratio of 2.8:1 (73.7% vs 26.3%)
average BMI of 34.20 kg/m2 (SD±8.79).
Using the Savary-Miller definitions, our patients displayed the following distribution alongside the endoscopic categorization of reflux disease:
11 (19.3 %) GERD 0 subjects,
13 (22.8%) GERD I subjects,
20 (35.1%) GERD II subjects,
7 (12.3%) GERD III subjects, and
6 (10.5%) GERD IV subjects
The population mean of AHI used as a direct measure of the severity of sleep apnea was 40.8 (SD±35.18). The patients were divided into two groups according to the severity of sleep apnea:
“mild-moderate” (A)-AHI 5-30, n = 27 and
“severe” (B)-AHI >30, n = 30.
The percentage of female patients was 37% in group A and 16% in B. The BMI was significantly higher in group B than in group A (P = 0.0002). There was no significant difference between two groups in respect of typical reflux symptoms (52% vs 47%), but in 50.5% of the study population these symptoms were negative (poor) according to our determination. When the endoscopic findings of GERD were analyzed, a higher frequency of severe cases was found in group B (P = 0.0001). In group A the incidence of GERD 0 was one-third of the cases, whereas in group B that was only 7%.
We compared the clinical (sleep) parameters and GER- related symptoms in each grade of GERD (Table 3). No significant difference was found between grades in respect of age, gender and GER-related symptoms. A positive correlation could be found between the severity of GERD and BMI. A very close connection was demonstrated between the severity of GERD and AHI values and the scores of Epworth scale.